A Drosophila model of Alzheimer's disease (AD) has been reported (Iijima et al., PNAS 101 (17): 6623-6628, 2004; Iijima et al., PLoS ONE 3(2): e1703, 2008), in which pan-neuronal expression of a secretary form of Aβ42 leads to phenotypes that recapitulate major features of AD clinical symptoms, including age-dependent memory loss, neurodegeneration, and accumulation of Aβ deposits. A subsequent study of synaptic plasticity in the Drosophila model of AD has revealed that long-term depression (LTD) is affected due to expression of Aβ42 (Chiang et al., FASEB J. 23: 1969-1977, 2009). A separate study also suggests that Aβ42-induced LTD resulted from an altered PI3 kinase activity (Chiang et al., PNAS 107: 7060-7065, 2010).